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Increases in plasma cyclic AMP dependent on endogenous catecholamines.

S Kunitada, M Honma, M Ui

    European Journal of Pharmacology
    |March 15, 1978
    PubMed
    Summary
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    Tyramine, ether anesthesia, and insulin hypoglycemia significantly elevate plasma cyclic AMP in rats. This indicates catecholamines activate adenylate cyclase via beta-adrenoceptors, with adrenal hormones and glucagon playing key roles in specific stress responses.

    Area of Science:

    • Pharmacology
    • Neuroendocrinology
    • Biochemistry

    Background:

    • Plasma cyclic AMP (cAMP) levels reflect adrenergic activity.
    • Understanding the regulation of cAMP is crucial for studying stress responses.

    Purpose of the Study:

    • To investigate the role of catecholamines and other hormones in elevating plasma cAMP under various stress conditions.
    • To elucidate the specific pathways involved in stress-induced cAMP increases.

    Main Methods:

    • Administration of tyramine, ether anesthesia, and insulin hypoglycemia in rats.
    • Treatment with pharmacological agents like reserpine, 6-hydroxydopamine, cocaine, and propranolol.
    • Assay of plasma cyclic AMP levels.

    Main Results:

    Related Experiment Videos

    • Tyramine, ether anesthesia, and insulin hypoglycemia sharply increased plasma cAMP.
    • Reserpine, 6-hydroxydopamine, cocaine, and propranolol blocked tyramine-induced cAMP increases, implicating sympathetic neuronal catecholamines and beta-adrenoceptors.
    • Adrenal catecholamines mediated cAMP increases during ether anesthesia.
    • Glucagon and adrenal catecholamines contributed to cAMP increases during hypoglycemia.

    Conclusions:

    • Sympathetic neuronal catecholamines activate adenylate cyclase via postsynaptic beta-adrenoceptors.
    • Adrenal medulla and glucagon play significant roles in stress-induced plasma cAMP elevation.
    • Plasma cAMP assays are promising for assessing adrenergic activity in research and clinical settings.